Exposure model chronic risk assessment

In Tables 14.9 and 14.10, the last column reports the environmental impact points (EIPs) for typical applications of organic and conventional pesticides derived from the Pesticide Environmental Assessment System, or PEAS. This model produces relative rankings of risks based on defined use rates and use patterns (the formulation used to apply a pesticide, timing, target of the application, spray equipment used, etc). PEAS scores reflect an equal balancing of acute pesticide risks to farm workers, chronic risks via dietary exposure and exposures to birds, Daphnia and bees. 

In animal experiments exposures can be carefully controlled, and dose-response curves can be formally estimated. Extrapolating such information to the human situation is often done for regulatory purposes. There are several models for estimating a lifetime cancer risk in humans based on extrapolation from animal data. These models, however, are premised on empirically unverified assumptions that limit their usefulness for quantitative purposes. While quantitative cancer risk assessment is widely used, it is by no means universally accepted. Using different models, one can arrive at estimates of potential cancer incidence in humans that vary by several orders of magnitude for a given level of exposure. Such variations make it rather difficult to place confidence intervals around benefits estimations for regulatory purposes. Furthermore, low dose risk estimation methods have not been developed for chronic health effects other than cancer. The... 

This model has a straightforward structure and is simple to use. It is based on studies carried out in part for the specific purpose of model development. However, not all of the required information is publicly available. The databases are not described at the study level the exposure data are only available in classes, although more detailed information is available on request. The choice of the statistics is not discussed. In the risk-assessment approach, some steps are not clearly presented. Sub-chronic toxicity studies, and not chronic toxicity studies, are used in the risk assessment. Exposure duration and frequency considerations are not discussed. Route-to-route extrapolation is considered acceptable implicitly, without further evaluation of the various issues involved. The rationale for using a dermal absorption default of 10 %, in the absence of data, is not discussed. 

Deterministic models are used to estimate chronic, or long-term, dietary exposures. Although research is currently being conducted on the use of distributional techniques for chronic dietary risk assessment, the author is not aware of any working model at this time. 

These criteria are selected by the Office of the Army Surgeon General as the most appropriate oral toxicity reference values for use in environmental risk assessments, and represent the Army s position (Opresko etal, 2001). The RfDg values have been input to USEPA risk models along with accepted chronic vapor exposure limits (as cited in Watson and Dolislager, 2007) to generate agent-specific... 

Poirier MC, Beland FA. 1992. DNA adduct measurements and tumor incidence during chronic carcinogen exposure in animal models implications for DNA adduct-based human cancer risk assessment. Chem. Res. Toxicol. 5 749-55... 

The development of biotic ligand models is in progress. The possibility of calculating the bio-availability of metals in the aquatic compartment is still under discussion and the validity of this approach still needs to be assessed for more species and for chronic exposures (Bonnomet and Alvarez, 2006). However, the EU has used BLM in the framework of Regulation No. 793/93 for the risk assessment of zinc. Based on these considerations it was decided that these parameters should be included in the reporting template, although they are not mandatory at the present stage. 

Occupational and toxicological studies have demonstrated adverse health effects from exposure to toxic contaminants. Emissions data from stationary and mobile sources are used in an atmospheric dispersion model to estimate outdoor concentrations of 148 toxic contaminants for each of the 60,803 census tracts in the contiguous United States for 1990. Approximately 10% of all census tracts had estimated concentrations of one or more carcinogenic HAPs at a greater than l-in-10,000 risk level. Twenty-two pollutants with chronic toxicity benchmark concentrations had modeled concentrations in excess of these benchmarks, and approximately 200 census tracts had a modeled concentration 100 times the benchmark for at least one of these pollutants. This comprehensive assessment of air toxics concentrations across the United States indicates hazardous air pollutants may pose a potential public health problem (Woodruff et al., 1998). 

Renal cell cultures have an unexploited potential in the screening and evaluation of possible nephrotoxins. These systems are theoretically suited not only to short term studies but also to long term exposures and thus may be useful in the screening of compounds on a chronic basis. Predictive models of chronic renal toxicity would be a major development in the assessment of human risk to a whole range of environmental, therapeutic and industrial compounds. However, if this is to be achieved successfully a number of requirements must be met. 

The approach discussed by Verhaar et al. (1997) suggests that development of PBPK/PD models to use in assessing health risks from TPH will require similar focusing on relevant lumping schemes, exposure pathways and durations, and toxicological effects and mechanisms of action. Thus, it is likely that a PBPK/PD model developed to aid in the assessment of potential cancer risk from chronic exposure to TPH may substantially differ from a PBPK/PD model for assessing risk for potential neurological effects from acute exposure to TPH. 

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